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Quick Reference
  • Normal Range: 3.5-5.0 mEq/L
  • Critical Values: <2.5 or >6.5 mEq/L
  • Primary Use: Cardiac monitoring, neuromuscular function assessment
  • Sample Type: Serum (venous blood) - avoid hemolysis
  • Hypokalemia: <3.5 mEq/L - causes U waves, arrhythmias
  • Hyperkalemia: >5.5 mEq/L - causes peaked T waves, cardiac arrest risk
  • Key Point: ECG changes more important than absolute value; always get ECG if abnormal K

Test Description

What is Potassium?

Potassium is the primary intracellular cation in the body.

Potassium Distribution

  • Intracellular: 98% of total body potassium (inside cells)
  • Extracellular: Only 2% of total body potassium (in serum/plasma)
  • Measured value: Serum potassium reflects only the small extracellular fraction

Why Is Potassium Tightly Regulated?

Serum potassium concentration is tightly regulated (3.5-5.0 mEq/L) because:

  • Small deviations = big problems: Even minor changes outside the narrow range can be life-threatening
  • Cardiac risk: Abnormal potassium causes dangerous arrhythmias
  • Neuromuscular risk: Affects muscle and nerve function throughout the body

Critical Functions of Potassium

  • Cardiac conduction: Maintains resting membrane potential; critical for normal cardiac rhythm
  • Neuromuscular excitability: Essential for nerve impulse transmission and muscle contraction
  • Cellular metabolism: Required for protein synthesis, glycogen formation, enzyme function
  • Acid-base balance: Participates in hydrogen ion exchange
  • Insulin secretion: Required for normal pancreatic beta-cell function
Critical Concept

Both hypokalemia and hyperkalemia can cause fatal arrhythmias. Severe potassium disturbances (K <2.5 or >6.5 mEq/L) with ECG changes constitute medical emergencies requiring immediate intervention.

Clinical Significance

Test Description

What is Potassium?

Potassium is the primary intracellular cation in the body.

Potassium Distribution

  • Intracellular: 98% of total body potassium (inside cells)
  • Extracellular: Only 2% of total body potassium (in serum/plasma)
  • Measured value: Serum potassium reflects only the small extracellular fraction

Why Is Potassium Tightly Regulated?

Serum potassium concentration is tightly regulated (3.5-5.0 mEq/L) because:

  • Small deviations = big problems: Even minor changes outside the narrow range can be life-threatening
  • Cardiac risk: Abnormal potassium causes dangerous arrhythmias
  • Neuromuscular risk: Affects muscle and nerve function throughout the body

Critical Functions of Potassium

  • Cardiac conduction: Maintains resting membrane potential; critical for normal cardiac rhythm
  • Neuromuscular excitability: Essential for nerve impulse transmission and muscle contraction
  • Cellular metabolism: Required for protein synthesis, glycogen formation, enzyme function
  • Acid-base balance: Participates in hydrogen ion exchange
  • Insulin secretion: Required for normal pancreatic beta-cell function
Critical Concept

Both hypokalemia and hyperkalemia can cause fatal arrhythmias. Severe potassium disturbances (K <2.5 or >6.5 mEq/L) with ECG changes constitute medical emergencies requiring immediate intervention.

Hypokalemia (K <3.5 mEq/L)

Hypokalemia is common, affecting up to 20% of hospitalized patients. It results from inadequate intake, transcellular shifts, or excessive losses (renal or GI).

Classification by Severity

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Severity Potassium Level Clinical Features
Mild 3.0-3.5 mEq/L Usually asymptomatic; fatigue, muscle weakness may occur
Moderate 2.5-3.0 mEq/L Muscle weakness, cramps, constipation, polyuria, ECG changes
Severe <2.5 mEq/L Severe weakness, paralysis, ileus, rhabdomyolysis, arrhythmias

Causes of Hypokalemia

1. Transcellular Shift (K Moves Into Cells)

  • Insulin: Promotes K uptake into cells (DKA treatment, insulin overdose)
  • Beta-2 agonists: Albuterol, epinephrine, stress/catecholamine surge
  • Alkalosis: Metabolic or respiratory alkalosis drives K into cells
  • Refeeding syndrome: Insulin surge with refeeding after starvation
  • Hypothermia: Intracellular shift during cooling
  • Hypokalemic periodic paralysis: Rare genetic disorder

2. Renal Losses (Urine K >15-20 mEq/L)

Diuretics (Most Common):

  • Loop diuretics (furosemide, bumetanide)
  • Thiazide diuretics (hydrochlorothiazide, chlorthalidone)

Mineralocorticoid Excess:

  • Primary hyperaldosteronism (Conn's syndrome)
  • Cushing's syndrome (excess cortisol has mineralocorticoid activity)
  • Licorice ingestion (glycyrrhizic acid inhibits 11β-HSD, mimics aldosterone)

Renal Tubular Disorders:

  • Renal tubular acidosis (Type 1 and Type 2)
  • Bartter syndrome, Gitelman syndrome (genetic)
  • Fanconi syndrome

Other:

  • Hypomagnesemia (impairs K retention; must correct Mg to correct K)
  • Amphotericin B (nephrotoxic)
  • Osmotic diuresis (hyperglycemia, mannitol)

3. GI Losses (Urine K <15 mEq/L)

  • Diarrhea: Most common GI cause (K-rich stool)
  • Vomiting/NG suction: Direct HCl loss + secondary hyperaldosteronism from volume depletion
  • Laxative abuse: Chronic laxative use
  • Villous adenoma: Secretes K-rich fluid
  • VIPoma: Vasoactive intestinal peptide-secreting tumor causing severe diarrhea

4. Inadequate Intake

  • Malnutrition, anorexia nervosa
  • Alcoholism
  • Elderly with poor diet

Note: Inadequate intake alone rarely causes severe hypokalemia because kidneys can reduce K excretion to <15 mEq/day

ECG Changes in Hypokalemia

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K Level ECG Findings
3.0-3.5 mEq/L • Flattened T waves
• Prominent U waves (best seen in V2-V3)
2.5-3.0 mEq/L • ST depression
• T wave inversion
• Prolonged QT interval (actually QU interval)
<2.5 mEq/L • Severe ST depression
• Ventricular ectopy (PVCs)
• Risk of torsades de pointes, VT, VF

Treatment of Hypokalemia

Severe Hypokalemia Treatment (K <2.5 or Symptomatic)
  • IV potassium chloride: 10-20 mEq/hour via central line (max 40 mEq/hour for life-threatening arrhythmias)
  • Continuous cardiac monitoring: Required during rapid IV replacement
  • Check and replace magnesium: Hypokalemia refractory to replacement if Mg is low
  • Avoid dextrose-containing fluids: Insulin secretion will worsen hypokalemia

Mild-Moderate Hypokalemia:

  • Oral potassium: Preferred for K >2.5 mEq/L (20-40 mEq PO q6-8h)
  • IV potassium (peripheral): Max 10 mEq/hour via peripheral IV (causes phlebitis if faster)
  • Address underlying cause: Stop diuretics, replace magnesium, treat diarrhea
  • Dietary sources: Bananas, oranges, potatoes, spinach (adjunct, not primary treatment)

Hyperkalemia (K >5.5 mEq/L)

Hyperkalemia is less common than hypokalemia but more immediately life-threatening due to risk of fatal arrhythmias. It results from decreased renal excretion, transcellular shifts, or excessive intake.

Classification by Severity

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Severity Potassium Level Clinical Significance
Mild 5.5-6.0 mEq/L Usually asymptomatic; monitor and address cause
Moderate 6.0-7.0 mEq/L ECG changes likely; muscle weakness possible
Severe >7.0 mEq/L Medical emergency; high risk of cardiac arrest
Rule Out Pseudohyperkalemia First

Pseudohyperkalemia = falsely elevated K due to K release from cells during/after blood draw:

  • Hemolysis: Most common cause (pink/red serum)
  • Prolonged tourniquet time: Fist clenching, difficult draw
  • Thrombocytosis: Platelets >1,000,000/µL release K during clotting
  • Leukocytosis: WBC >100,000/µL (leukemia)

If suspected, repeat sample with careful technique. Patient will be asymptomatic and ECG normal.

Causes of Hyperkalemia

1. Decreased Renal Excretion (Most Common)

Kidney Disease:

  • Acute kidney injury (AKI) - most common true cause
  • Chronic kidney disease (CKD) with GFR <20 mL/min
  • End-stage renal disease (ESRD)

Medications (Very Common):

  • RAAS inhibitors: ACE inhibitors, ARBs, direct renin inhibitors
  • Potassium-sparing diuretics: Spironolactone, amiloride, triamterene
  • NSAIDs: Decrease renin and aldosterone
  • Heparin: Decreases aldosterone synthesis
  • Trimethoprim, pentamidine: Block renal K secretion
  • Calcineurin inhibitors: Tacrolimus, cyclosporine

Hypoaldosteronism:

  • Addison's disease (primary adrenal insufficiency)
  • Type 4 RTA (hyporeninemic hypoaldosteronism) - common in diabetics

2. Transcellular Shift (K Exits Cells)

  • Acidosis: Metabolic acidosis (K shifts out as H+ moves in)
  • Insulin deficiency: DKA, hyperglycemic hyperosmolar state
  • Cell lysis: Tumor lysis syndrome, rhabdomyolysis, hemolysis, burns
  • Hyperkalemic periodic paralysis: Rare genetic disorder
  • Beta-blockers: Non-selective beta-blockers impair cellular K uptake
  • Succinylcholine: Causes K release from muscle (avoid in burns, denervation)
  • Digitalis toxicity: Inhibits Na-K-ATPase pump

3. Excessive Intake

  • IV potassium administration (error, too rapid infusion)
  • Salt substitutes (KCl-based) in renal patients
  • Potassium-rich foods in CKD/ESRD (rare alone)
  • Massive blood transfusion (stored blood has high K)

ECG Changes in Hyperkalemia

ECG changes progress as K rises and are more predictive of cardiac risk than absolute K level:

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K Level ECG Findings
5.5-6.5 mEq/L • Tall, peaked T waves (narrow base)
• Shortened QT interval
6.5-7.5 mEq/L • PR prolongation
• P wave flattening/loss
• QRS widening
7.5-8.0 mEq/L • Marked QRS widening
• "Sine wave" pattern (pre-arrest rhythm)
>8.0 mEq/L • Ventricular fibrillation
• Asystole
• Cardiac arrest

Treatment of Hyperkalemia

EMERGENCY Treatment (K >6.5 or ECG Changes)

IMMEDIATE ACTIONS (Cardioprotection):

  1. Calcium gluconate 10%: 10-20 mL IV over 2-3 min
    • Stabilizes cardiac membrane (no effect on K level)
    • Effect within 1-3 minutes, lasts 30-60 min
    • Repeat if ECG changes persist

SHIFT K INTO CELLS (Temporary Measures):

  1. Insulin + Dextrose: 10 units regular insulin IV + 25g dextrose (D50W)
    • Lowers K by 0.5-1.5 mEq/L
    • Onset 15-30 min, peak 30-60 min, duration 4-6 hours
    • Monitor glucose (risk of hypoglycemia)
  2. Albuterol: 10-20 mg nebulized (or 0.5 mg IV)
    • Lowers K by 0.5-1.0 mEq/L
    • Onset 30 min, duration 2-4 hours
    • Synergistic with insulin
  3. Sodium bicarbonate: 50-100 mEq IV (only if severe metabolic acidosis present)
    • Questionable efficacy as sole agent
    • Use in acidotic patients (pH <7.1)

REMOVE K FROM BODY (Definitive Therapy):

  1. Loop diuretics: Furosemide 40-80 mg IV (if adequate renal function)
    • Increases renal K excretion
    • Ineffective in oliguric AKI or ESRD
  2. Potassium binders:
    • Sodium polystyrene sulfonate (Kayexalate): 15-30g PO/PR (onset 1-2 hours, slow)
    • Patiromer (Veltassa): 8.4-25.2g PO daily (non-acute, for chronic hyperkalemia)
    • Sodium zirconium cyclosilicate (Lokelma): 10g PO TID (faster onset than patiromer)
  3. Hemodialysis: Most effective method
    • Indications: Severe hyperkalemia refractory to medical therapy, AKI/ESRD, K >7.5-8.0 mEq/L
    • Removes 25-50 mEq K per hour

Mild Hyperkalemia (5.5-6.0 mEq/L, No ECG Changes):

  • Dietary potassium restriction (<2g/day)
  • Discontinue offending medications (ACE-I, ARBs, K-sparing diuretics, NSAIDs)
  • Loop diuretics if adequate renal function
  • Treat underlying cause (optimize renal function, correct acidosis)
Clinical Pearls
  • "Peaked T waves = hyperkalemia until proven otherwise": Tall, narrow-based, symmetric T waves are the earliest and most specific ECG finding.
  • ECG trumps lab value: A K of 6.2 with peaked T waves is more concerning than K of 7.0 with normal ECG. Treat based on ECG changes, not just the number.
  • Hypokalemia + diuretics = dangerous arrhythmia risk: Diuretic-induced hypokalemia significantly increases risk of ventricular arrhythmias, especially in patients on digoxin or with structural heart disease.
  • Hypokalemia is often accompanied by hypomagnesemia: Mg deficiency impairs renal K conservation. Always check and replace Mg when treating hypokalemia. "K won't stay up until Mg is corrected."
  • Refractory hypokalemia? Think Mg, Mg, Mg: If K replacement isn't working, check magnesium level and replace aggressively (2-4g MgSO4 IV).
  • ACE-I + ARB + spironolactone = "triple whammy" for hyperkalemia: Combining RAAS inhibitors dramatically increases hyperkalemia risk, especially in CKD.
  • Hemolyzed sample? Repeat before treating: Pink or red serum indicates hemolysis, causing pseudohyperkalemia. Repeat with careful draw. Never treat based on hemolyzed sample alone.
  • DKA presents with hyperkalemia, then hypokalemia: Initial hyperkalemia (acidosis, insulin deficiency) masks total body K depletion. K drops precipitously with insulin treatment. Monitor closely and replace early.
  • Calcium doesn't lower potassium: Calcium stabilizes cardiac membrane but has zero effect on serum K. It buys time for definitive therapy (insulin, dialysis) to work.
  • Sine wave = cardiac arrest imminent: Wide, sine wave-like QRS pattern on ECG indicates extreme hyperkalemia. Give calcium immediately and prepare for crash cart/dialysis.
  • Avoid rapid K correction for chronic hypokalemia: Chronic hypokalemia allows cellular adaptation. Rapid correction can cause rebound hyperkalemia, especially in renal impairment.
  • Loop diuretics are useless in anuric patients: Furosemide requires urine output to work. In oliguric AKI or ESRD, dialysis is the only reliable method to remove K.
  • Normal K doesn't mean normal total body K: Serum K represents <2% of total body K. A patient can have severe total body K depletion with normal serum K (and vice versa during transcellular shifts).
References
  1. Kratz, A., Ferraro, M., Sluss, P. M., & Lewandrowski, K. B. (2004). Laboratory reference values. New England Journal of Medicine, 351, 1548-1564.
  2. Lee, M. (Ed.). (2009). Basic skills in interpreting laboratory data. Ashp.
  3. Farinde, A. (2021). Lab values, normal adult: Laboratory reference ranges in healthy adults. Medscape. https://emedicine.medscape.com/article/2172316-overview?form=fpf
  4. Nickson, C. (n.d.). Critical Care Compendium. Life in the Fast Lane • LITFL. https://litfl.com/ccc-critical-care-compendium/
  5. Farkas, Josh MD. (2015). Table of Contents - EMCrit Project. EMCrit Project. https://emcrit.org/ibcc/toc/
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